ArticleDer Orthopade2009
[Osteoblasts : cellular and molecular regulatory mechanisms in fracture healing].
Article in Der Orthopade, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Complement Proteins C1q-C5 as Context‑Dependent Regulators of Osteoblast Function and Fracture Healing: A Systematic Review.Orthopedic reviews · 2026Article
- The osteogenic potential of human bone callus.Scientific reports · 2016Article
- Article
- The expanding world of tissue engineering: the building blocks and new applications of tissue engineered constructs.IEEE reviews in biomedical engineering · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone tissue possesses a unique regeneration ability, translating mechanical and metabolic stimuli into a biological response. The perpetual regeneration processes allow continuous self-renewal and adaptation to prevailing mechanical forces. The complex regulation of osteoblastic differentiation during fracture repair has not been completely defined. Two different transcription factors - RUNX2 and SP7 - are considered to be master genes of osteoblastic differentiation. Furthermore, the canonical WNT pathway plays an essential role in the activation of osteoblastic differentiation during both bone growth and fracture healing. Studies of fracture healing have revealed that downregulation of the WNT pathway causes a significant reduction in new bone formation. Moreover, correct WNT signalling is also required for BMP2-induced bone formation. There is increasing evidence that patients who develop recalcitrant fracture nonunions exhibit not only reduced numbers and differentiation capacity of osteogenic progenitors but also a significant downregulation of numerous factors in the WNT pathway. Therefore, better understanding of the WNT regulatory mechanisms could reveal new strategies for the treatment of delayed fracture healing and for the tissue engineering of bone.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.